The human LV is a thick-walled chamber (average approximately 1.0 cm at ED) with a truncated ellipsoid shape composed of spiraling, sheetlike layers of myocyte bundles (Fig. 3-15). The orientation of the bundles changes from subepicardium to subendocardium, progressing from relatively longitudinal (in relation to the long axis of the ellipsoid) to roughly circumferential fibers occupying about the middle two-thirds of the wall to longitudinal fibers once again in the subendocardium.^ Regional wall thickness parallels the local radius of curvature. Near the apex, where the radius is small, thickness is relatively small. Variations in thickness may function to equalize regional wall stress.

Figure 3-15: Three-dimensional architecture of LV, illustrating spiraling bundles of myofibers (see text). (From Streeter.i^2 Reprinted with permission of the publisher.)

Contraction of the LV is associated with a wringing motion, or torsion, characterized by a counterclockwise rotation that progressively increases from base to apex.1^3 Torsion is important for normal ejection and is an inherent feature of the normal spread of excitation and the connections between the fiber bundles.104 It also is likely a storage mechanism for potential energy generated during systole that is converted to kinetic energy during diastole, assisting filling by suction.1^5 This complex architecture results in efficient conversion of the shortening of individual myocytes and fibers to wall thickening, which is ultimately responsible for ejection of blood. Thus, even though individual fibers shorten only about 10 percent, the normal LV ejects about two-thirds of its ED volume. Interventricular septal fibers have a similar orientation and are continuous with those of the LV free wall. As a result, the septum normally functions as a part of the LV; i.e., during contraction, its endocardial surface undergoes more or less symmetric inward movement toward the center of the LV.

In line with the high-capacitance/low-resistance nature of the pulmonary vascular bed, the RV is much thinner-walled than the LV (3 to 4 mm in an adult human) and appears crescentic in cross section.1^2 Its contraction has been likened to that of a bellows. The RV inflow and outflow portions are functionally distinct, with inflow contraction preceding outflow contraction.1^6 A significant fraction of the mechanical output of the RV appears to be related to energy transfer from the LV through the interventricular septum (systolic ventricular interaction).107 This is supported by the observation that destruction of much of the free wall of the RV is remarkably well tolerated.

Ventricular myocardium also has a well-developed connective tissue matrix.108-110 Cardiac collagen is organized into a weave of fibers that forms a netlike structure around the myofibers (groups of six or more myocytes), as well as connections that link adjacent myofibers and strutlike projections connecting to adjacent blood vessels. The latter may function to help maintain vessel patency during contraction. The collagen network of the ventricles is an important determinant of their passive filling properties (see discussion below). The last major component of the ventricles is the vascular bed, described below.

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